p90 RSK (Phospho-Thr359+Ser363) ELISA Kit

Name: p90 RSK (Phospho-Thr359+Ser363) ELISA Kit
SKU: DEIA-XYA1397
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

cultured cells

Species Reactivity

Human; Mouse; Rat

Intended Use

The p90 RSK (Phospho-Thr359+Ser363) Colorimetric Cell-Based ELISA Kit allows for the qualitative detection of p90 RSK (Phospho-Thr359+Ser363) and the effects that certain stimulation conditions have on p90 RSK (Phospho-Thr359+Ser363) expression in different cell lines.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate: 2 Plates.
2. 10x TBS: 24 mL (10x), Clear.
3. Quenching Buffer, 24 mL (1x), Clear.
4. Blocking Buffer, 50 mL (1x), Clear.
5. 10x Wash Buffer, 50 mL (10x), Clear.
6. 100x Anti-p90 RSK (Phospho-Thr359+Ser363) Antibody (Rabbit Polyclonal) 60 μL (100x) Red.
7. 100x Anti-p90 RSK Antibody (Rabbit Polyclonal) 60 μL (100x) Purple.
8. 100x Anti-GAPDH Antibody (Mouse Monoclonal) 60 μL (100x) Green.
9. HRP-Conjugated Anti-Rabbit IgG Antibody, 12 mL (1x), Glass.
10. HRP-Conjugated Anti-Mouse IgG Antibody, 12 mL (1x), Glass.
11. Primary Antibody Diluent, 12 mL (1x), Clear.
12. Ready-to-Use Substrate, 12 mL (1x), Brown.
13. Stop Solution, 12 mL (1x), Clear.
14. Crystal Violet Solution, 12 mL (1x), Glass.
15. SDS Solution, 24 mL (1x), Clear.
16. Adhesive Plate Seals, 4 Seals.

Storage

4°C/6 Months

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Negative feedback via RSK modulates Erk-dependent progression from naive pluripotency

EMBO REPORTS

Authors: Nett, Isabelle R. E.; Mulas, Carla; Gatto, Laurent; Lilley, Kathryn S.; Smith, Austin

Abstract

Mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) signalling is implicated in initiation of embryonic stem (ES) cell differentiation. The pathway is subject to complex feedback regulation. Here, we examined the ERK-responsive phospho-proteome in ES cells and identified the negative regulator RSK1 as a prominent target. We used CRISPR/Cas9 to create combinatorial mutations in RSK family genes. Genotypes that included homozygous null mutations in Rps6ka1, encoding RSK1, resulted in elevated ERK phosphorylation. These RSK-depleted ES cells exhibit altered kinetics of transition into differentiation, with accelerated downregulation of naive pluripotency factors, precocious expression of transitional epiblast markers and early onset of lineage specification. We further show that chemical inhibition of RSK increases ERK phosphorylation and expedites ES cell transition without compromising multilineage potential. These findings demonstrate that the ERK activation profile influences the dynamics of pluripotency progression and highlight the role of signalling feedback in temporal control of cell state transitions.

Genomic profiling of Sezary syndrome identifies alterations of key T cell signaling and differentiation genes

NATURE GENETICS

Authors: Wang, Linghua; Ni, Xiao; Covington, Kyle R.; Yang, Betty Y.; Shiu, Jessica; Zhang, Xiang; Xi, Liu; Meng, Qingchang; Langridge, Timothy; Drummond, Jennifer; Donehower, Lawrence A.; Doddapaneni, Harshavardhan; Muzny, Donna M.; Gibbs, Richard A.; Wheeler, David A.; Duvic, Madeleine

Abstract

Sezary syndrome is a rare leukemic form of cutaneous T cell lymphoma characterized by generalized redness, scaling, itching and increased numbers of circulating atypical T lymphocytes. It is rarely curable, with poor prognosis. Here we present a multiplatform genomic analysis of 37 patients with Sezary syndrome that implicates dysregulation of cell cycle checkpoint and T cell signaling. Frequent somatic alterations were identified in TP53, CARD11, CCR4, PLCG1, CDKN2A, ARID1A, RPS6KA1 and ZEB1. Activating CCR4 and CARD11 mutations were detected in nearly one-third of patients. ZEB1, encoding a transcription repressor essential for T cell differentiation, was deleted in over one-half of patients. IL32 and IL2RG were overexpressed in nearly all cases. Our results demonstrate profound disruption of key signaling pathways in Sezary syndrome and suggest potential targets for new therapies.